Our results revealed that the phase separation of tau under physiological conditions may be initialized by the intrinsically disordered N-terminal inserts of tau and subsequently combined with aggregation-prone C-terminal MTBR, which may stabilize tau condensates to undergo a liquid-to-solid phase transition [7] and to result in pathological tau aggregation and further neurofibrillary tangles in neurodegenerative diseases. The gene discussed is MAPT; the disease is neurodegenerative disease.